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相关概念视频

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
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The Thyroid Gland01:23

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The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
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空间转录学揭示了转录学和免疫微环境在甲状腺癌分化过程中的重编程

Kang Ning1,2,3, Bu Zou1,2,3, Yongchao Yu1,2,3

  • 1Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

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概括
此摘要是机器生成的。

无塑性甲状腺癌 (ATC) 通过基因组变化和免疫抑制从差异化甲状腺癌 (DTC) 演变. 损失的PDCD4驱动瘤相关的巨细胞透,对于ATC的进展至关重要.

关键词:
M2巨细胞其他类型甲状腺瘤的发生分化甲状腺癌空间转录学

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科学领域:

  • 癌症学
  • 基因组学
  • 免疫学

背景情况:

  • 甲状腺癌 (ATC) 是一种高度致命的恶性瘤.
  • 甲状腺癌通常是由差异化甲状腺癌 (DTC) 引起的,原因是人们对甲状腺癌的分化过程不太了解.

研究的目的:

  • 阐明推动从DTC到ATC的分子机制.
  • 确定甲状腺癌分化中的关键调节者和细胞参与者.

主要方法:

  • 在共存的DTC和ATC区域上进行空间转录组测序 (spRNAseq).
  • 整体外体测序和推断CNV分析
  • 轨迹分析和机械实验.

主要成果:

  • ATC表现出高调的免疫抑制,血管生成和ECM重塑基因.
  • 邻近的DTC区域显示早期的基因组变化,
  • PDCD4和TYMP是甲状腺癌脱差的关键调节剂.
  • 瘤相关的巨细胞 (TAMs) 富含ATC,促进免疫抑制.
  • 通过eIF4A依赖的途径促进了PDCD4的透.

结论:

  • 具有ATC样基因组变化的DTC经历了转录和免疫重编程,成为ATC.
  • 由PDCD4损失引起的TAM形成对ATC的发展和进展至关重要.